A major premise of the GRC series has been that much of the cancer associated with environmentally-induced and endogenous DNA damage is linked to damage-induced mutagenesis. Cells use a network of interconnected pathways to suppress mutagenesis and carcinogenesis. They repair damaged DNA and bypass DNA-replication-blocking lesions by processes that balance efficiency and fidelity. Damage-triggered signaling pathways delay cycling of genetically-compromised cells and may eventually eliminate them. The 2008 conference will place a strong emphasis on consequences for human health. A pair of keynote talks that describe the "genetic landscapes" of cancer will set the stage for sessions concerned with specific genetic alternations in cancer cells and on the genetic epidemiology of sporadic cancer. Other health-related sessions focus on cellular responses to chemotherapy-induced DNA damage that may induce secondary cancers and expand consideration of consequences of processing of damaged DNA to tissue growth and development and aging. Selected talks will emphasize the value of new model systems - Arabidopsis and Zebrafish - to the DNA repair and mutagenesis community. Sessions more concerned with the molecular starting points of damage-processing will focus on the structural biology and theory of DNA-damage recognition and expand the definitions of damage to include novel structures in lesion-free DNA and sequence context effects. Core sessions will aim at biochemical understanding of the balance between error-prone vs. high-fidelity responses blocked replication forts. One will describe successive steps in pathways initiated by specific DNA lesions. [unreadable] [unreadable] [unreadable] [unreadable]